Clinical observations have accumulated which suggest that a delay of ovulation, when the follicular phase of the menstrual cycle is prolonged, often results in defective embryonic development, abortions and birth defects. Studies from this laboratory in an animal model have shown a high incidence of abnormal embryonic development following either an induced or a spontaneous delay of ovulation. Results indicate that the intrafollicular oocyte is altered during the delay of ovulation. Measurements of gonadotropins and steroid hormones during delayed ovulation suggest that an early rise and continued elevation of estrogen in relation to the time of ovulation could be responsible for alterations of the oocyte and result in birth defects. The present research using the rat as a model will test this hypotheses by producing a delay in ovulation and at the same time block the early rise in estrogen. If estrogen is responsible for alterations of the oocyte, the high incidence of abnormalities previously produced by an equal period of delay in ovulation in this species should be prevented. Alterations of ultrastructure of the oocyte by estrogen will be studied. Embryo transfer will be used to examine the effects of age and estrous-cycle length in old rats on the oocyte and uterine environment.